Outline

It is well recognized that different cells, tissues and organs are differently radiation sensitive. To categorize radiosensitive versus radioresistant structures one has to consider the specific endpoint (e.g. early reaction versus late reaction; radiation induced tumor induction versus radiation necrosis), follow-up time (in case of late reactions), and co-factors. These classifications are well accepted among radiation oncologists and radiobiologists and widely applied in practice. However, the mechanisms underlying the different radiosensitivity of different tissues, and of different endpoint in the same tissue are often unknown. The target cell hypothesis postulated that, as a consequence of DNA damage, target cells are inactivated by radiation which leads to depletion of these cells causing radiation damage. In this model the severity of damage correlates with the degree of target cell inactivation. The time interval before damage becomes detectable is dependent on both, the degree of inactivation and the turn over times of the tissues. However, investigations performed in the last two decades indicate that several other intracellular targets beside of DNA may be influenced by radiation. For some of these targets an influence on radiation sensitivity of cells and tumors could be demonstrated. The presentation will summarize the current knowledge of different targets for low and high radiation doses in cells and tissues.